Skip Navigation


MBE Advance Access originally published online on July 3, 2006
Molecular Biology and Evolution 2006 23(10):1902-1911; doi:10.1093/molbev/msl050
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Supplementary Material
Right arrow All Versions of this Article:
23/10/1902    most recent
msl050v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (7)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Suzuki, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Suzuki, Y.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2006. Published by Oxford University Press on behalf of the Society for Molecular Biology and Evolution. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Research Article

Natural Selection on the Influenza Virus Genome

Yoshiyuki Suzuki

Center for Information Biology and DNA Data Bank of Japan, National Institute of Genetics, Mishima-shi, Shizuoka-ken, Japan

E-mail: yossuzuk{at}lab.nig.ac.jp.

Influenza viruses are the etiological agents of influenza. Although vaccines and drugs are available for the prophylaxis and treatment of influenza virus infections, the generation of escape mutants has been reported. To develop vaccines and drugs that are less susceptible to the generation of escape mutants, it is important to understand the evolutionary mechanisms of the viruses. Here natural selection operating on all the proteins encoded by the H3N2 human influenza A virus genome was inferred by comparing the numbers of synonymous (dS [DS]) and nonsynonymous (dN [DN]) substitutions per site. Natural selection was also inferred for the groups of functional amino acid sites involved in B-cell epitopes (BCEs), T-cell epitopes (TCEs), drug resistance, and growth in eggs. The entire region of PB1-F2 was positively selected, and positive selection also appeared to operate on BCEs, TCEs, and growth in eggs. The frequency of escape mutant generation appeared to be positively correlated with the dN/dS (DN/DS) values for the targets of vaccines and drugs, suggesting that the amino acid sites under strong functional constraint are suitable targets. In particular, TCEs may represent candidate targets because the dN/dS (DN/DS) values were small and negative selection was inferred for many of them.

Key Words: influenza virus • genome • positive selection • negative selection • vaccine • drug


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Mol Biol EvolHome page
S. L. Kosakovsky Pond, A. F.Y. Poon, A. J. Leigh Brown, and S. D.W. Frost
A Maximum Likelihood Method for Detecting Directional Evolution in Protein Sequences and Its Application to Influenza A Virus
Mol. Biol. Evol., September 1, 2008; 25(9): 1809 - 1824.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
S. Kryazhimskiy, G. A. Bazykin, and J. Dushoff
Natural Selection for Nucleotide Usage at Synonymous and Nonsynonymous Sites in Influenza A Virus Genes
J. Virol., May 15, 2008; 82(10): 4938 - 4945.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.